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BIO 200 CHPT. 11

QuestionAnswer
Resting membrane potential V sub r; inside is always negative and outside is always positive; -70mV; polarized; sodium & potassium ions are important for RMP
Graded potential signal that results from change in membrane potential; short distances
Action potential signal that results from change in membrane potential; longer distances
Hyperpolarization inhibits AP; membrane potential changes towards negative (goes in a more neg. direction) ex: -70mV>>-80mV
Polarized differences in ion concentration
Sodium is always _____ inside and ______ outside sodium is always LOW inside and HIGHER outside
Calcium is always _______ inside and _________ outside Calcium is always SUPER LOW inside and HIGHER outside
Potassium is always ___________ inside and ________ outside Potassium is always HIGH inside and LOWER outside
Two ways to change the RMP from -70mV change membrane permeability and change ion concentration
Changing membrane permeability any ion (allows ions to cross the membrane that don't normally cross it); changes RMP
Changing ion concentration changes RMP; intracellular or extracellular
Depolarization required for AP; membrane potential changes towards positive (from neg. to pos.); ex: from -70mV>>-60mV
What stimulates graded potentials? hyperpolarization or depolarization
For graded potentials, bigger stimulus means... bigger "graded potential"
Graded potentials decrease with... distance; localized current flow only
Afterhyperpolarization undershoot; final phase (4) of action potential
Absolute refractory VG Na+ channels open; no other stimulus (regardless of size) can trigger more APs
Relative refractory VG Na+ channels closed; VG K+ channels open; VERY LARGE stimulus will trigger an AP
Saltatory conduction transmission of an action potential along a myelinated fiber in which the nerve impulse appears to leap from gap to gap
Three parts to chemical synaptic junction 1) NT binds to NT receptor; 2) Opens NT/channel & negative ions move inside OR positive ions move inside; 3) Resulting graded potential is depolarization is (+) ion and is hyperpolarization if (-) ions
For graded potentials, where do ions flow into the cell? ONLY at the active site (like a channel)
Active current of graded potentials active site
Passive current of graded potentials ions flowing ALONG membrane surfaces (inside & outside) but not across membrane; redistribution of charge
Depolarization with graded potentials depolarization= (-) outside and (+) inside neighboring areas, continues along membrane surface (a reversal from when at rest)
Why can the graded potential occur? (3 important membrane properties) 1) Membrane insulates (no ions flow across, only along) 2) Fluids inside/outside conduct ion flow 3) membrane permeable to K+ (K+ leaks out of cell)
K+ leak channels K+ is always leaving cell via leaky channels so eventually depolarization will slow
Excitable cell examples neurons, skeletal muscle, cardiac muscle, and smooth muscle
Where does graded potential occur? ONLY in dendrites & cell body (axon to cell body and axon to dendrites)
Excitable cells have.. action potential
Action potential is a reversal of what? membrane potential; goes from -70mV>>+30mV which is depolarization
Three changes that occur to membrane permeability in action potential 1) increase in Na+ permeability 2) return to Na+ impermeability 3) increase in K+ permeability
What induces the membrane permeability in action potential? depolarization
Phase 1 of Action potentials Depolarization; open Na+ channels (activation gate) and Na+ flows in; permeability=high Na+/low K+; positive feedback so more channels open; depolarization of axon leads to more VG channels opening
Positive feedback in action potentials means all this spreads along the membrane and more channels can open
Phase 2 of action potentials VG (Na+) close (inactivation gate closes on Na+ channel); permeability=low N+ & K+; more (+) charge builds up on inside and channels close around 0mV
Phase 3 of action potentials Repolarization; VG (K+) open (K+ ions flow out of the cell); permeability=low Na+ and high K+; cell becomes less (+) as K+ leaves
Repolarization approaching resting conditions
Phase 4 of action potential Undershoot; continued K+ outflux; permeability=low Na+ and high K+; VG (K+) respond slowly stay open; resting ionic concentrations return as increase Na+/K+--ATPase activity
During an AP, what ion has the highest permeability during the "undershoot" phase? K+
Major difference between action potentials & graded potentials? AP=only involves ions (K+ & Na+) flowing into the cell via voltage gated channels and Graded potentials=passive flow of ions ALONG the membrane (except for where they flow in ONLY at the active site)
Propagation the spreading of something into new regions; i.e. how the AP moves along the axon
How does AP move along the axon? neighboring areas become depolarized & more VG Na+ channels open; AP moves along the axon and "self-propagating" continues along axon
Why does AP move only in one direction? (two reasons) - 1) increased density of VG Na+ channels (***main reason) - 2) refractory period of the Na+ channel (inactive)
Where does an AP start? at axon hillock
APs are generated by balance between what? Na+ entering the cell (depolarizing) and K+ leaving the cell (hyperpolarizing)
What if you have a SMALL STIMULUS for APs? only a few VG Na+ channels open & let in small amount of Na+; K+ leaves via leak channels and remains higher than Na+ entering which results in small depolarization below threshold (-55mV) so NO ACTION POTENTIAL OCCURS
Threshold for AP to occur? -55mV
What if you have a LARGE STIMULUS for APs? Many Na+ channels open letting in large amount of Na+ and then K+ leaves in lower amounts than the Na+ entering resulting in a large depolarization that goes above the threshold and ACTION POTENTIAL OCCURS
All-or-None concept of AP stimulus above threshold=AP; stimulus below threshold=NO AP
All APs are the same.... size (strength)
How is stimulus strength of APs transmitted? as frequency (rather than size); number of APs/unit of time; Bigger stimulus means more APs/unit of time
What two variables can affect AP conduction velocities? Axon diameter and myelin sheath
Axon diameter effect on AP conduction velocities Larger diameter, the faster the conduction rate due to smaller resistance to electrical (ion) flow
AP conduction velocity how fast the AP can move along the axon
Myelin Sheath effect on AP conduction velocities insulates axon which reduces charge leakage; myelinated axons allow for EVEN faster conduction compared to unmyelinated axons; leads to saltatory conduction
Multiple Sclerosis autoimmune disease; loss of myelin that often causes slowing movement of the eye, etc.
Axondendritic axon to dendrite synaptic connection
Axosomatic axon to cell body synaptic connection
Axoaxonic axon to axon synaptic connection
Dendrosomatic dendrite to cell body synaptic connection
Dendrodendritic dendrite to dendrite synaptic connection
Presynaptic neuron "sending" impulse towards the synapse
Postsynaptic neuron impulse away from synapse; "receiving"
Botox blocks the release of neurotransmitter acetylcholine from neuromuscular junction so presynaptic cell can’t release the NT to the muscle
Excitatory Postsynaptic Potentials (EPSPs) depolarization in the postsynaptic cell; Na+ & K+ flow thru a single NT receptor channel
Inhibitory Postsynaptic Potentials (IPSPs) K+ and/or Cl- permeability increased--NT receptor channel; Causes hyperpolarization & reduces MP; will not cause an AP at axon (OR) increases the size of the depolarization that you would need to fire an AP
Temporal summation presynaptic neuron releases NT in rapid sequence on a postsynaptic neuron; produces larger depolarization
Spatial summation one than another presynaptic neuron stimulated at the same time; many NT receptors activated at once; larger depolarization (basically, you have two presynaptic neurons stimulated at the same time so you have larger reaction/depolarization)
Post-tetanic potentiation enhancement occurs after repeated stimulation or "tetanic stimulation"; enhancement can continue even after stimulation stopped (termed post-tetanic stimulation)
Acetylcholine helps with muscles; Neuromuscular junction NT (between neurons & muscles); can be excitatory (neuromuscular junctions) or inhibitory (cardiac)
Biogenic amines Catacholamines; serotonin, dopamine, & epinephrine; NT
Catacholamines serotonin, dopamine, & epinephrine; NT
Serotonin catacholamine; NT
Dopamine catacholamine; NT
Epinephrine catacholamine; NT
Glutamate amino acids; NT; depolarization (excitatory); involved in stroke/seizures
Gamma-aminobutyric acid (GABA) amino acid; NT; hyperpolarization (inhibitory)
Endorphins Peptides; NT
Substance P Peptides; NT
Ionotropic receptors channel-linked receptors; for direct action to open an ion channel; rapid response, localized, & brief
Metabotropic recptors G-protein-linked NT receptors; for indirect action via second messenger; slow response, prolonged, & complex
Facilitated zone Subthreshold stimulation; stimulation from other sources can induce AP
Discharge zone closely linked to presynaptic input; likely to reach threshold
Divergence (circuits) Amplification; single sensory receptor; up spinal cord & multiple brain regions at once
Convergence (circuits) opposite of divergence; multiple presynaptic inputs; concentrated effect; increases response; results in multiple stimuli causes the same response
Reverberating circuit signal comes in, but goes around back & forth in a cycle; could drive something like heart beat or breathing; they generate constant cycles/repeating things
Parallel circuit one signal in, but takes multiple pathways to get an output; ex: problem solving; information goes thru multiple circuits at one time, problem solving circuit, etc. so we are capable of putting information through multiple circuits at one time;
Parallel processing inputs into many different pathways (processed simultaneously); one stimulus travels thru multiple pathways & can cause multiple unique response; for higher mental function
5 types of synaptic connections axondendritic, axosomatic, axoaxonic, dendrosomatic, dendrodendritic
Two types of synaptic junctions in PNS neuromuscular junctions & neuroglandular junctions
Neuromuscular junctions neuron to muscle; synaptic junction of PNS
Neuroglandular junctions neuron to gland cell; synaptic junction of PNS
Two classes of synapses electrical & chemical synapse
Electrical synapse gap junctions (direct, not chemical, cytoplasmic connections; neuron-neuron); very rapid
Chemical synapse most common junction; release & receive chemical signals; slower signal mechanism; via neurotransmitters;
Two parts of chemical synapses axonal terminal & receptor region
Axonal terminal of chemical synapse; transmitting neuron; presynaptic neuron; synaptic vesicles with NT (bags containing NTs)
Receptor region of chemical synapse; receiving; postsynaptic neuron; NT receptors
Synaptic cleft space between pre & post synaptic neurons
Presynaptic cell chemical synapse mechanism (2 steps) Electrical signal at axon terminal --depolarization --opens VG Na+ & Ca2+ channels (*[Ca2+]) 2) NT released by exocytosis --synaptic vesicles fuse w/membrane --Release NT to synaptic cleft
Postsynaptic cell chemical synapse mechanism (2 steps) 3. NT binds to NT receptor (postsynaptic neuron) 4. NT/NT receptor channels open Conformational change - opens Ion current flow changes membrane potential (graded) Excitation or inhibition
Higher frequency of APs at the presynaptic cell= bigger effect in postsynaptic cell; and more NT released
How do drugs affect NT release? Drugs (toxins) block the release of NT from the presynaptic cell Blocks release of the vesicle containing the NT
Three ways the chemical synaptic response can be turned off 1) enzymes can degrade NTs 2) reuptake of NT 3) just gets diluted and diffuse out of synaptic cleft
Small stimulus at postsynaptic cell no AP occurs as K+ flows out (leak channels) and prevents excessive (+) charge inside the cell
Large stimulus at postsynaptic cell EPSPs move down dendritic process/cell body to axon hillock=graded potential; generates an AP down the axon
Which type of synaptic junction is faster--chemical or electrical junction? electrical (gap junction) because it's a direct link
EPSPs can "summate" meaning... add together; multiple EPSPs on a single postsynaptic neuron so you're more likely to reach threshold--induce an AP
If you have EPSP+IPSP.... =lower depolarization (very slight depolarization because they kinda equal each other out)
How does the axon hillock integrate all EPSPs and IPSPs? determines response (threshold or sub-threshold); closer presynaptic terminal is to axon hillock, greater the influence; example of graded potential
Repeated activation of a synapse results in... postsynaptic neuron is more easily stimulated (called synaptic potentiation)
Three criteria for NT 1) present presynaptic terminal & released with stimulation 2) NT applied to postsynaptic neuron produces response (EPSP or IPSP) 3) natural mechanism exists to terminate response
Two types of messengers (recently described NTs) ATP & nitric oxide
Direct NT mechanism bind to receptor and open ion channel (ACh does this)
Indirect NT mechanism bind to receptor, activate G-protein; activate second messenger; activate/deactivate ion channel; (i.e. serotonin)
Two zones of neuronal pools facilitated zone & discharge zone
Circuits pattern of connection of neuronal pools
Four types of circuits divergence, convergence, reverberating, parallel
Serial processing predictable all-or-none manner; a reflex; stimulus goes through one pathway and then has a response in effector organ
Order of serial processing receptor>sensory neuron>CNS integration>motor neuron>effector (muscle)
Two types of neuronal processing Serial processing & parallel processing
Created by: amay322
 

 



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